Altered cholesteryl ester cycle is associated with lipid accumulation in herpesvirus-infected arterial smooth muscle cells.

TitleAltered cholesteryl ester cycle is associated with lipid accumulation in herpesvirus-infected arterial smooth muscle cells.
Publication TypeJournal Article
Year of Publication1985
AuthorsHajjar DP, Falcone DJ, Fabricant CG, Fabricant J
JournalJ Biol Chem
Volume260
Issue10
Pagination6124-8
Date Published1985 May 25
ISSN0021-9258
KeywordsAnimals, Arteries, Cells, Cultured, Chickens, Cholesterol, Cholesterol Esters, Lipid Metabolism, Marek Disease, Muscle, Smooth, Vascular
Abstract

We describe herein the effects of Marek's disease herpesvirus (MDV) on cholesterol and cholesteryl ester metabolism in cultured chicken arterial smooth muscle cells. Infection of arterial smooth muscle cells from specific pathogen-free chickens with MDV, but not a virus control, herpesvirus of turkeys led to a 7-10-fold increase in the accumulation of free and esterified cholesterol and a 2-fold increase in phospholipids. The cellular lipid changes observed in the MDV-infected arterial smooth muscle cells resulted, in part, from the following: decreased low-density lipoprotein-cholesteryl ester hydrolysis due to decreased lysosomal (acid) cholesteryl ester hydrolytic activity; increased de novo synthesis of cholesterol; decreased excretion of free cholesterol; and, both increased cholesteryl ester synthetic activity and decreased cytoplasmic (neutral) cholesteryl ester hydrolytic activity which resulted in increased incorporation of oleic acid into cholesteryl ester. Other changes noted in the MDV-infected cells as compared to uninfected cells included a 2-fold increase in both total protein synthesis and lysosomal and microsomal marker enzyme activities. These alterations in lipid and protein metabolism in MDV-infected arterial smooth muscle cells may explain in part our in vivo findings that herpesvirus (MDV) infection of specific pathogen-free chickens fed a normocholesterolemic diet will induce arterial thickening and lipid accumulation resembling human atherosclerosis.

Alternate JournalJ Biol Chem
PubMed ID3997816
Grant ListHL-18828 / HL / NHLBI NIH HHS / United States
HL-19381 / HL / NHLBI NIH HHS / United States
HL-28179 / HL / NHLBI NIH HHS / United States
Related Faculty: 
David P. Hajjar, Ph.D. Domenick J. Falcone, Ph.D.

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